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More importantly, this molecular shift is observed in 3-weeks old mice, before the main features of Tau pathology, defined by the appearance of abnormal and hyperphosphorylated Tau aggregates, that occurs in 6 to 10 months-old mice.
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To determine whether this molecular shift was dependent on phosphorylation of PDE3B, HA-PDE3B was co-expressed in Cos-1 cells along with IKKε, TBK1 or their kinase inactive mutants, and HA immunoprecipitates were treated with or without calf intestinal phosphatase (CIP).
So, after molecular docking, its shift is negligible: in the case of HL2 + C60, the Rmsd value for C60 fullerene is 3.99 Å (for HL2 1.36 Å), and in the case of C60 + HL2 2.7 Å (for HL2 3.29 Å).
Thus, no significant molecular weight shift was expected.
Since the thickness of our cantilever is much larger than that of molecular monolayer, the resonant frequency shift is related to mass of molecules.
Molecular modelling indicates that this functional shift is principally attributable to a single charge altering amino acid substitution in the β-type δ-globin chain (δ136Gly→Glu) of this species that perturbs electrostatic interactions between the dimer subunits via formation of an intra-chain salt-bridge with δ82Lys.
The molecular mechanism by which this large Stokes shift is induced is currently not well understood.
The shift is consistent with that observed for aromatic molecular crystals.
The shift is independent of the wavelength of excitation, which means that the energy shift is constant for each separate molecular species.
The shift is disorienting.
The shift is telling.
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